Ati Cardiovascular System Meds (Cardiac Glycosides And Heart Failure)

Front 1

cardiac glycosides

Back 1

digoxin (Lanoxin, Lanoxicaps, Digitek)

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cardiac glycosides MOA

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positive inotropic effect- increased force of myocardial contraction
increased force and effeciency of myocardial contraction improves the heart's effectiveness as a pump; improving stroke volume and cardiac output

negative chronotropic effect= decreased heart rate
at therapeutic levels, digoxin slows the rate of SA node depolarization and the rate of impulses through the conduction system of the heart
decreased heart rate gives the ventricles more time to fill with blood coming from the atria which leads to increased SV and increased CO

Front 3

cardiac glycosides use

Back 3

treatment of heart failure
dysrhythmias (atrial fibrillation)

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cardiac glycosides adverse

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dysrhythmias- digoxin-induced dysrhythmias include hypokalemia, increased serum digoxin levels, and HD. Older adult clients are particularly at risk
cardiotoxicity leading to bradycardia
GI effects
CNS effects

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cardiac glycosides contraindications

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pregnancy category risk C
disturbances in ventricular rhythm, including ventricular fibrillation, ventricular tachycardia, and second and third degree heart block
hypokalemia, partial AV block, advanced heart failure, and renal insufficiency

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cardiac glycosides interactions

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thiazide diuretics, such as HCTZ, and loop diuretics suchas furosemide (Lasix), may lead to hypokalemia, which increases the risk of developing dysrhythmias

ACE inhibitors and ARBs increase risk of hyperkalemia, which can lead to decreased therapeutic effects of digoxin

sympathomimetic medication such as dopamine (Intropin) compelemnt the inotropic actio nof digoxin and increase the rate and force of heart muscle contraction
increase risk of tachydysrhymias
quinidine increases risk of digoxin toxicity when used concurrently
verapamil (Calan) increases plasma levels of digoxin
antacids decrease absorption of digoxin and can decrease its effectiveness

Front 7

cardiac glycosides admin

Back 7

notify provider if pulse rate is less than 60/BPM
less than 70 BPM in child
monitor digoxin levels periodically during treatment and maintain therapeutic levels between 0.5 to 2.0 ng/mL to prevent digoxin toxicity
If administering IV digoxin infuse over 5 min, and monitor for dysrhythmias

Front 8

management of digoxin toxicty

Back 8

digoxin and potassium sparing meds should be stopped immediately
Monitor K+ levels
treat dysrhythmias with phenytoin (Dilantin) or lidocaine
treat bradycardia with atropine
for excessive overdose, activated charcoal, cholestyramine, or Digibind can be used to bind digoxin and prevent absorption

Front 9

cardiac glycosides effectiveness

Back 9

control of heart failure
absence of cardiac dysrhythmias

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adrenergic agonist

Back 10

proto: catecholamines
epinepherine (Adrenaline)
dopamine (Intropin)
dobutamine

others:
isoproterenol: cataecholamine
terbutaline: noncatechlamine

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alpha 1 (adrenergic agonists) MOA

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activation of receptors in the arterioles of the skin, viscera and mucous membranes, and veins leads to vasoconstriction

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beta 1 (adrenergic agonist) MOA

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heart stimulation leads to increased heart rate, increased myocardial contractility, and increased rate of conduction through the AV node
Activation of receptors in the kidney lead to the release of renin

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beta 2 (adrenergic agonist) MOA

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activation of receptors in the arterioles of the heart, lungs, and skeletal muscles leads to vasodilation
bronchial stimulation leads to bronchodilation
activation of receptors in uterine smooth muscle causes relaxation
activation of receptors in the liver cause glycogenolysis
skeletal muscle receptor activation leads to muscle contraction

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dopamine (adrenergic agonist) MOA

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activation of receptors in the kidney cause the renal blood vessels to dilate

Front 15

alpha 1 (adrenergic agonist) use (epinepherine)

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vasoconstriction
slows absorption of local anesthetics
manages superficial bleeding
decreased congestion of nasal mucosa
increased BP

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beta 1 (adrenergic agonist) use (epinepherine)

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increased heart rate, increased myocardial contractility, increased rate of conduction through the AV node
treatment of AV block and cardiac arrest

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beta 2 (adrenergic agonist) use (epinepherine)

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bronchodilation
treats asthma

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dopamine (adrenergic agonist) use

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renal blood vessel dilation (low dose)

renal blood vessel dilation, increased heart rate, increased myocardial contractility, increased rate of conduction through the AV node (moderate dose dopamine, beta 2)

renal blood vessel constriction
increased heart rate
increased myocardial contractility
increased rate of conduction through AV node
vasoconstriction
(High dose: dopamine, beta1, alpha 1)
treats shock, heart failure

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dobutamine (adrenergic agonist) use (beta 1)

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increased heart rate
increased myocardial contractility
increased rate of conduction through AV node
treats heart failure

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epinepherine adverse

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vasoconstriction from activation of alpha 1 receptors in the heart can lead to hypertensive crisis

beta 1 receptor activation in the heart can case dysrhythmias
beta 1 receptor activation also increases the workload of the heart and increases oxygen demand, leading to development of angina

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dopamine adverse

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beta 1 receptor activation in the heart can cause dysrhythmias
beta 1 receptor activation also increases the workload of the heart and increases oxygen demand, leading to the development of angina
necrosis can occur from extravasation of high doses of dopamine

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dobutamine adverse

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increased HR

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adrenergic agonist contraindications

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epinepherine and dopamine are pregnancy category C
dobutamine is category b
tachydysrhythmias and ventricular fibrillation
hyperthyroidism, angina, history of MI, hypertension and diabetes

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adrenergic agonist interactions

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MAOIs
TCAs
anesthteics can cause heart to become hepersenstive to the effects of epinepherine, leading to dysrhythmias
alpha-adrenergic blocking agents such as phentolamine, block action at alpha receptors
beta-adrenergic blocking agents such as propranolol
diuretic promote beneficial effects of dopamine

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adrenergic agonist admin

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IV pump to control infusion
dosage is titrated based on BP response
stop infusion of dopamine at first evidence of infiltration
extravasation can be treated with local injection of an alpha-adrenergic blocking agent, such as phentolamine
assess for chest pain
monitor urine output frequently for signs of decreased renal perfusion

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adrenergic agonist effectiveness

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improved perfusion as evidenced by urine output of greater than or equal to 30 mL per hour with normal renal function, improved mental status, and systolic BP maintained at greater than or equal to 90 mmHG